Shell-shock and other neuropsychiatric problems
Part 17
He was sent that evening to the neuropsychiatry center, walking jerkily and as if slightly drunk, with a number of small gesticulations and murmurings. He was immediately isolated, undressed himself and went to bed. He did not move in his bed, and seemed to sleep. The next day he got up, dressed and had a small spell of excitement, but was quiet enough on the medical visit, though the floor was soiled with urine and vomitus and the clothing was in disorder. He now had a pronounced phase, deep sunk eyes, drawn features and anxious look; dilated pupils and an expression of mixed fear and anger. His breathing was hard and he kept his hand on his heart. He was oriented. He suddenly rose and said, “I am thirsty.” A glass of milk was given him. He hesitated a moment, plunged his mouth and hands into it and aspirated the drink without making any swallowing movements. He pushed away the glass, spat a little, and vomited a small quantity of a black liquid. Then followed an anxious crisis, and he fell upon his side, absolutely immobile, without breathing for a few seconds. Again in the sitting posture, he was taken with contractions of the limbs and face. The tendon reflexes were at this time normal.
A quarter of an hour later the attendant found him dead, in the sitting posture, leaning against the wall, mouth open, arms dependent, hands extended, pupils dilated--a death in syncope. The brain was found congested. There was a slight effusion of blood over the posterior aspect of the brain. There were no hemorrhages or softenings in the brain substance. The muscles were of a dark red to black. The adherent lungs were very slightly congested at the base. The stomach contained a quarter of a liter of black, inodorous fluid in which there was much bile and little blood. There were numerous small hemorrhages of the mucosa near the great curvature. The spleen was large, the liver congested. The Pasteur Institute confirmed the diagnosis of rabies. There is no history of the man’s having been bitten by a dog.
Tetanus: Psychosis.
=Case 119.= (LUMIÈRE AND ASTIER, 1917.)
A soldier wounded May 18, 1916, was given antitetanic serum May 26th. The wounds healed, but on June 16, that is, 29 days after the trauma, contractures began, at first localized. There had been numerous wounds of legs and scrotum by shell fragments and the contractures were limited to the right leg and scrotum. There was no trismus or any lumbar symptom.
During the next few days the contractures became general, the temperature rose, a shell fragment was found by X-ray at the root of the thigh and was surgically extracted. B. tetani was found upon inoculation of media with material from the shell fragment. Persulphide of soda and antitetanic serum 90 cc. in three days were given intravenously. The temperature fell and the general health was greatly improved. July 6, hallucinations and terrors, worse at night, set in. The man believed himself surrounded by flames, that daggers were being plunged into his old wounds, that his hair was being pulled. These symptoms lasted a fortnight only, whereupon the patient recovered.
This case and six others accompanied by cerebral disturbances all recovered, and all the patients retained a perfect memory of their delirium and of their hallucinations.
The chronological distribution of these cases was odd. One case was found early in the war; then no other cases of cerebral disorder presented themselves until the group observed at the end of 1916. Besides flames and daggers, zoöpsia was several times observed. One of the cases showed these symptoms without having been given antitetanic serum.
_Re_ tetanus in the war, see in the _Collection Horizon_ a book by Courtois-Suffit and Giroux on _Les formes anormales du tétanos_.
Tetanus fruste versus hysteria.
=Case 120.= (CLAUDE AND LHERMITTE, 1915.)
Claude and Lhermitte describe a condition of _tetanos fruste_. The neck was absolutely rigid. The patient had not been wounded in any way and, being regarded as a pure neuropath, was sent to the Centre Neurologique at Bourges.
The differential diagnosis lay between true tetanus and the hysterical pseudotetanus or pseudomeningitis. In pseudotetanus there is a contracture of the superficial and deep neck muscles, especially the trapezii, sternomastoid, and deep muscles. The condition somewhat suggests that of acute meningitis or tetanus, and especially suggests tetanus because it is often associated with masseter contracture (hysterical trismus). The head is immobile, stiff, and inclined backward; eyes directed above, throat slightly prominent. Upon attempts to move the head, intense pain occurs. The pain and contracture sometimes even suggest a suboccipital Pott’s disease. This form of hysterical pseudotetanus is of sudden onset, as a rule following burial in a trench or else contusion, or a slight wound in the cervical region. Pressure on the spinous processes produces no pain, nor does a blow upon the head; and an X-ray examination will definitely eliminate the hypothesis of Pott’s disease.
To return to the Claude-Lhermitte case of limited true tetanus: It showed marked modifications in the tendon and bone reflexes. Upon percussion of the zygoma, of the occiput, or of the clavicle, there was a marked further contraction in the contractured muscles. Although there was no apparent spasticity in the legs, there was an ankle clonus and a bilateral patella clonus, combined with a distinct exaggeration of all bone and tendon reflexes. In such cases also there is hyperexcitability of the nerves and muscles to faradic and galvanic currents.
An officer’s letter concerning local tetanus.
=Case 121.= (TURRELL, January, 1917.)
The following letter from an officer who had had local tetanus and was treated by Turrell by ionization Dec. 6 and 7, 1915, by diathermia Dec. 7 to 22, and occasionally by static breeze ionization and chlorine ion to relieve contractions from Dec. 29, 1915, to Feb. 4, 1916. The tetanus was in the muscles of the legs. Of course diathermia is a purely symptomatic treatment and does not replace antitoxin serum or other specific treatment; thus its effect in relieving the contractions of local tetanus is precisely like its effect in the treatment of sciatic neuritis or lumbago.
November 15, 1916.
“Dear Major Turrell,
“I have been meaning to write to you for some time, as I knew you would be interested to hear how I was getting on. Your letter has just been received, and I am only too happy to give you any information I can with regard to my leg. I was wounded in the left leg on October 13, 1915, by high explosive shell, and arrived at Oxford on October 22. There was no operation as the surgeon in charge did not consider it advisable to remove the pieces of shell: my leg seemed to be getting better, and after about a month I was able to hobble round with sticks. My foot at this time used to swell a great deal towards night, and the foot seemed then to gradually stiffen up with violent pains at intervals, this gradually spread up the whole leg to about the knee, and I was compelled to take to my bed again. The pain at times was very bad, similar to a very bad attack of cramps, and then my leg became rigid and stiff, and at other times used to get horrible jumps and it was impossible to keep it still, and whenever the doctor or nurse looked at it it used to stiffen up at once. The night seemed to be the worst, and consequently I got very little sleep. I often had to get up in the middle of the night on crutches to try and obtain relief, my leg was so cramped and sore. It was about this time that you first visited me and prescribed a course of electric treatment for my leg, and I shall never be able to thank you enough for the relief it gave me. I cannot remember the names of the different treatments, but the first one--diathermy, or heat pads--certainly relieved the pain, and after the first two or three visits to you I got immense relief. I never looked back after this, and, although the progress was slow, I gradually lost all pain and was able to get sleep at night. The nervous jumps slowly disappeared and my leg became gradually normal except for contraction of the tendons. I was unable to straighten my ankle or knee, and it was thought at one time that my tendo Achillis would have to be severed. Gradually the knee straightened and I was able to get my heel to the ground. I was for some time on crutches, and was able to leave the hospital on February 5, 1916, walking with sticks.… I am now able to walk comfortably, but am unable to flex the ankle more than at right angle to my leg. The circulation is not very good, and I feel anything tight round my calf. I am still getting Boards, and have not been passed fit for overseas yet.”
VI. SOMATOPSYCHOSES
(THE SYMPTOMATIC, NON-NERVOUS, GROUP)
Dysentery: Psychosis.
=Case 122.= (LOEWY, November, 1915.)
Out of a large number of dysentery patients, many of whom had very serious symptoms, but one of Loewy’s patients became psychotic. Loewy in fact had discharged this one as normal, and he had been put on the wagon train (no opium or alcohol) to go to a sanatorium. As the fighting shifted, the sanatorium site changed and could not be reached with the wagon. Finally, the wagon train met the battalion once more and Loewy was told that the man was “dying.” At this time he was afebrile, without collapse symptoms, with a strong and normally frequent pulse, and with few signs of exhaustion. Yet the guard had thought that he looked moribund. Both upper eyelids were drawn rigidly up but conveyed a different impression from that in maniacal or anxious conditions. The expression was that of staring astonishment, helplessness, and apathetic lack of orientation. The patient recognized Loewy, spoke to him as “Herr Doctor,” said he was doing quite well; he was found to be well oriented. There was no fabricating tendency even as to the number of stools (although Loewy had noted such in bad dysenteries of the _Shiga-Kruse_ type). He was apparently hard of hearing, as if at the beginning of a typhoid fever. He showed a retardation in his intake of ideas, and his voice in answering sounded absent-minded. There was an expression of absent-mindedness, and the patient seemed markedly unconcerned about his health, the direction of the journey, the terrible rain, etc. These phenomena are attributed by Loewy to attention disorder.
The patient had been out of reach of fire for days. Loewy reports the case as one of beginning amentia or as an exhausted state resembling a Korsakow condition, recalling one of emotional hyperesthetic weakness (Bonhoeffer).
Typhoid fever: Hysteria.
=Case 123.= (STERZ, December, 1914.)
A soldier entering hospital for typhoid fever, October 2, 1914, was discharged to another hospital and again, November 10, to a hospital for nervous disease. The typhoid was serious and complicated by delirium. After defervescence, the patient was weak and could not stand or walk, especially on account of pains and weakness in the left leg. Sometimes he had had pains in the sacrum and left hip. He complained of tinnitus, deafness, dizziness, headache. He said he had fallen from a cart, had been sick for three months, since which time he had been under medical treatment for his present condition. He had, he said, been given a small pension.
The gait disorder sometimes amounted to a real astasia-abasia. The left leg became stiff and was dragged behind. There was a paresis demonstrable in dorsal decubitus, of the left side, especially of the leg, without atrophy. There was a hypesthesia of the whole left side of the body, with the exception of the head. Hyperesthesia of the left leg, hip and upper sacrum. The left corneal reflex was diminished. Moody, hypochondriacal, lachrymose. The general attitude of the patient was affected and theatrical. Paradoxical innervations were frequently found on test. There was no neurological disorder except for the absence of the right Achilles jerk.
The absence of this Achilles jerk may be regarded as a residuum of the previous accident. The localization of the pains points to a neurotic lumbosacral plexus disorder on the left side. Superimposed upon this picture are the hysterical phenomena. The typhoid fever and its attendant neuritis are therefore to be interpreted as the liberating factor for a severe hysteria in a subject already disposed to such symptoms through previous accident.
Dementia praecox versus post-typhoidal encephalitis.
=Case 124.= (NORDMAN, June, 1916.)
A butcher, 29 (aunt insane, sister melancholy, one child stillborn, deformed), had had several days convulsions at eight; went through military service without incident; was at the Marne and was evacuated October 19, 1914, with typhoid fever,--a severe fever with a delirium prolonged into the last weeks. Three months convalescent leave was given, passed at Paris with the man’s aunt, but he had become strange. One day he wanted to strangle neighbors of German origin; another day departed for Dunkirk and then returned, having lost all his documents.
February, 1915, he went back to the front, did strange things and was soon evacuated to Tarascon. In April he went back to his dépôt; May 18, to the hospital at Rennes for erythema. June 15, he was given 15 days in prison for setting off a cannon too quickly and then running off through the fields. August 11, he was interned at Rennes for stealing a priest’s cap. September 12, two months convalescence. December 10, headaches. Back to Rennes January 14, February 18, Val-de-Grâce, then Maison Blanche.
Here he was found sometimes sad, immobile; at other times laughing and singing. He was very irritable on small occasion. Once on leave he had a fugue with complete amnesia, though alcohol may account for the latter. His memory was vague, especially for his crimes and for recent events. He was emotional, indifferent even in the presence of his wife or aunt. Sexual indifference. He often complained of his head, saying that he felt it blocked and that he could not think. The headache was frontal and would last several hours. The man would, however, not complain spontaneously. He was physically, in general, negative.
This case might possibly be due to a post-typhoidal encephalitis, but Nordman believes rather that it is a case of dementia praecox. Perhaps the convulsions at eight produced a slight brain lesion, brought to an issue by the typhoid fever.
Paratyphoid fever: Psychosis outlasting fever.
=Case 125.= (MERKLEN, December, 1915.)
A Breton farmer, 34, had paratyphoid alpha. Admitted to hospital September 3, 1915, he had headache, anorexia, asthenia, coated tongue and tense abdomen, algosuria; later, abdominal swelling, borborygmi in the right iliac fossa, rose spots, dicrotism, albuminuria, bronchitic rales. The disease was severe, and was complicated by sacral decubitus and ran a month.
At first somnolent, September 8th the patient went into a state of mental excitement with agitation and delirium. He got out of bed, cried out, sang, talked to his neighbors, complained that his papers (colis) had been stolen, as well as his watch and tobacco; that his horses’ hoofs had been injured, and the like.
He grew calmer in a few days, and now no longer tried to get up, remaining inert in his bed. The occupation delirium persisted--he was not being paid what he owed, and the like. He had hallucinations; looked for scissors, and one day said, “Here they are!” At intervals he appeared lucid and responded appropriately to questions.
The fever dropped and the paratyphoid disease appeared past, but the mental state remained for three weeks without change, having the same periods of lucidity when he would be regarded as cured, but falling again forthwith into his post oniric ideas. He was soon sent to a convalescent hospital and was not wholly well for another month.
Psychopathic taint brought out by paratyphoid fever.
=Case 126.= (MERKLEN, December, 1915.)
A soldier, 31, was a victim of paratyphoid alpha, entering hospital October 21, 1915, with the usual symptomatology: fever, asthenia, headache, abdominal swelling, tongue coated and red along its edges, diarrhoea. After admission he passed into a deep toxic state.
He woke up in the night with a cry, got up afraid, and refused to go back into his own bed. He was mute, except for curses addressed to the nurses. After two hours he went to bed and to sleep. Next day he sat quietly with a depressed look, occasionally groaning deeply, talking in brief phrases about his anxiety, wanting his wife telephoned to, saying that he would not see his children, was going into the four planks, and the like.
This situation lasted about a week. He became afraid of medicines and thought he had been poisoned, saying that he would rather be shot than poisoned and complaining that, though he had served France for fourteen months, they now wanted to kill him. In the night time he was agitated. He gave vent to cries, and threats, but this delirious state rapidly decreased and he became calm the night of September 27th. The upper extremities showed a tendency to catatonia. From this time forth, during the remaining month, the patient was immobile, mute, fearful, and mistrusting, depressed and always wore a cunning look. His disorientation decreased and he passed good nights. He would answer questions by groaning. He would say, “They think I am a Tartar.” The end of the mental disorder coincided with the cure of the paratyphoid fever. According to Merklen, the paratyphoid bacillus in these cases serves to bring out a psychopathic taint. This particular patient had always been of a sad demeanor, uncommunicative, very impressionable and emotional. Two other cases had always been somewhat below normal.
Diphtheria: Post-diphtheritic symptoms.
=Case 127.= (MARCHAND, 1917.)
A farmer, 37, was evacuated March 20, 1916, for diphtheria. April 1, paralysis of tongue and uvula, impairment of vision. These symptoms rapidly improved, but paralysis of the legs appeared and then of the arms. This paralysis lasted until he was sent to the neurological center June 28 for post-diphtheritic paralysis, wherein it was found that voluntary movements of the legs could be performed, though painfully and of slight extent, that walking was impossible, that there was a considerable atrophy of legs and arms, that the knee-jerks, Achilles jerks and plantar reflexes were absent. There was complaint of pains in the legs and over nerve trunks.
Improvement followed, the atrophy gradually passed away, and the voluntary movements of the legs became more extensive; but by October the reflexes had not yet reappeared. Yet the patient had begun to walk on crutches and soon was able to get on with canes only. The improvement did not continue. He did not raise his heels and dragged his toes. There was now a clonic tremor of the legs as soon as the weight of the body was put on them. During movements of legs carried on in dorsal decubitus there was found an irregular tremor of the legs with twisting of the trunk. The muscular strength was well preserved. There was a slight muscular atrophy. The tendon reflexes had now come back, though the right Achilles jerk was weak and the plantar reflexes were absent. There was a hypalgesia of the legs which ceased sharply at the middle of the thighs. There was a slight hypoacusia on the left side. Visual fields normal. The patient complained of feelings in the inside of his bones. Electrical reactions normal.
Diphtheria: Hysterical paraparesis.
=Case 128.= (MARCHAND, 1917.)
A soldier, 24, was evacuated June 24, 1915, from Roussy for diphtheria and was treated by serum, receiving 80 cc. in 8 injections. A few days later there was a paralysis of the uvula with regurgitation of liquids from the nose; but patient was able to go on convalescence July 21. A few days later, however, he noticed that his legs were weak. Vertigo, vomiting and painful walking followed, and his convalescence was increased a month. The paralysis got progressively worse. September 10, he went by automobile to Libourne where he stayed two months. He arrived at the Neurological Center at Bordeaux November 9 with diagnosis “polyneuritis of legs.” He could not walk and could hardly flex thighs on pelvis or legs on thighs. Voluntary movements of extension and flexion of feet and toes were limited. There was neither atrophy, pain nor reflex disorder. Both legs were analgesic, as was also the abdomen up to the umbilicus. There was complaint of dorsolumbar pains and of stomach trouble and lack of appetite; vomiting after meals frequent, pulse 120.
January 3, the patient was able to lift his legs a few centimeters above the bed but not together. There was now a slight muscular atrophy especially on the left side. Knee-jerks lively, analgesia limited to legs, no vomiting, pulse rapid.
The patient was sent to a hospital in the country May 8 to July 8. He was now much better. His legs were able to support his body but he could not walk. Slight atrophy of left leg. There was hypalgesia now in the feet and legs below the knee. There was no pain on pressure over the nerve trunks. The electric reactions normal. The patient could now walk on crutches. He was invalided on the temporary basis, December 12, 1916.
It does not appear that in this case the hysterical paralysis was preceded by polyneuritis.
Malaria: Amnesia.
=Case 129.= (DE BRUN, November, 1917.)
A soldier lost all memory of his hospital stay in Salonica and the voyage home. He could only remember a little about the hospital at Bandol. There is a period of transition to full memory in malarial cases characterized by sure memory, vague on certain points, alternating with phases of almost complete amnesia. The soldier in question had very inexact memories of the Bandol Hospital, and could only remember about his fevers, that they began about noon and terminated about four o’clock. Twice he had been found in his shirt, walking, unconscious, in the passageway of the hospital. Having obtained leave for convalescence, three months after his memory gap began, he went to Paris, and probably had attacks at home. He vaguely remembered afterward being carried by automobile to the Pasteur Hospital, December 1. There he remained to the end of March, 1917, without preserving anything but the vaguest memories of an intermediary period of more than six months. The memory in these malarial cases often remains permanently altered and there may even be a retrograde amnesia, carrying back to facts prior to the gap and an anterograde amnesia relative to facts after the main gap.
Thus, there is in the febrile period a retrograde amnesia and in the post-febrile period a retrograde or anterograde amnesia. One group of subjects are severe cerebral cases, and the memory gap appears to run back to a period of true mental confusion. But there is another group of patients who preserve throughout the febrile period an absolute consciousness of all acts, and yet the memory gap is just as sharp and definite as in the confusional cases.
Malaria: Korsakow syndrome.
=Case 130.= (CARLILL, April, 1917.)